The objectives of this proposed research are to describe the hemodynamic state of vascular beds in the various stages of experimental renal hypertension and to attempt to identify the chemical and/or physical factors responsible for these hemodynamics. Because elevated cardiac output and mesenteric blood flow occur in the early stages of renal hypertension, we will investigate the effects of chronic elevation of mesenteric blood flow on mesenteric hemodynamics, to test the hypothesis that the increased resistance in established hypertension represents "long-term autoregulation". In the hyperperfused mesenteric bed of normotensive mongrel dogs under pentobarbital anesthesia we will measure resistance, flow-pressure relationships, pressure-volume relationships, vascular responses, effects of maximal vasodilation, and vascular wall composition. Because we have indirect evidence suggesting that an abnormality in vascular Na-K activated ATPase may underlie the hemodynamic changes in renal hypertension, we will directly measure NA, K-ATPase activity in vessels from hypertensive animals. Finally, we plan to measure venous pressure-volume relationships, and Na, K-ATPase activity in vessels from essential hypertensive humans.